[62, 63] also reported that dysfunction of mitochondria was observed in peripheral blood lymphocytes of SLE patients and MRL/lpr mice, and that improving mitophagy by deletion of Rab4A or inhibition of the mTOR signaling facilitates the expands of CD4+T cells and reduces CD8+ T cells, thereby enhancing B cell activation, plasma cell development, antinuclear and antiphospholipid autoantibody production, and glomerulonephritis. Here, MTOR is linked to glomerulonephritis.